Topic
Lanosterol
About: Lanosterol is a research topic. Over the lifetime, 1239 publications have been published within this topic receiving 36737 citations. The topic is also known as: (3β)-lanosta-8,24-dien-3-ol & (3β,20R)-lanosta-8,24-dien-3-ol.
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TL;DR: Pentanorlanost-8-en-3β,22-diol has been isolated from the mycelium of the fungus Verticillium lecanii and addition of lanosterol to the culture medium did not significantly increase the yields either of the pentanor Lanostane metabolites or of ergosterol.
12 citations
TL;DR: In vitro tests showed that some of novel 1,2,3,4-tetrahydroisoquinoline derived azoles effectively inhibit the growth of several strains of yeasts as well as molds.
12 citations
TL;DR: The major triterpenols produced by in vitro cultures are campesterol, sitosterol, Δ5-avenasterol and α-amyrin, as they were identified by mass spectra of their trimethylsililated and acetylated derivatives.
12 citations
TL;DR: For instance, after 1-2 hours after intragastric administration of ketoconazole, a cytochrome P-450 inhibitor, to rats, there was a 50-60% decrease in the activity of hepatic 3-hydroxy-3-methylglutaryl-CoA reductase.
Abstract: At 1-2 h after intragastric administration of ketoconazole, a cytochrome P-450 inhibitor, to rats, there was a 50-60% decrease in the activity of hepatic 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) reductase. Inhibition reached a maximum at 6-12 h after the drug was given, but after 24 h enzyme activity was stimulated by 60%. The rates of synthesis of hepatic non-saponifiable lipids in vivo showed a similar time-dependent pattern of change. During the first few hours after drug administration, the hepatic cytochrome P-450-dependent metabolism of lanosterol was suppressed in vivo. However, 24 h after treatment, this activity was stimulated, an effect which was also observed by pre-treatment of the rats with the drug for several days. Suppression of hepatic HMG-CoA reductase and lanosterol 14 alpha-demethylase activities was accompanied by a relative increase in the accumulation of labelled polar sterols in the liver in vivo. In the intestine, ketoconazole also resulted in a rapid decline in the rate of synthesis of non-saponifiable lipids and an inhibition of lanosterol 14 alpha-demethylation in vivo. However, in contrast with the liver, there was no stimulation of non-saponifiable lipid synthesis after 24 h.
12 citations
TL;DR: The in vivo conversion, by the myxomycete, of differently labelled lanosterol, stigmastanol, and 5′-stigmast-22-en-3β-ol, into the sterols 12a 11a is described and the possible biosynthetic routes for the two sterols are discussed.
Abstract: Several laboratiories have shown that the two carbon atoms C-28 and C-29 of the ethyl or ethylidene side chains of phytosterols are introduced on to a C-24 unsaturated side chain by two methylation steps. A scheme based on previous work suggests the various intermediates which can be formed by stabilisation of the carbonium ion 3. We have shown previously that in the biosynthesis of 5′-stigmastan-3β-ol (11a) and 5′-stigmast-22-en-3β-ol (12a), sterols of the myxomycete Dictyostelium discoideum, routes h and i could be excluded.
In the present paper we describe the in vivo conversion, by the myxomycete, of differently labelled lanosterol (13), stigmastanol (11), and 5′-stigmast-22-en-3β-ol (12), into the sterols 12a 11a, and discuss the possible biosynthetic routes for the two sterols.
After incorporation of a mixture of [26,27-14C2]lanosterol and [24-3H]lanosterol (3H/14C = 5.60 ± 0.25), the isolated sterols 11a 12a were converted into 11b (3H/14C = 5.54 ± 0,28) and 14b (3H/14C = 5.61 ± 0.28).
By ozonisation followed by oxidation in neutral or basic medium, 12a was converted into the esters 15 (3H/14C = 5.54 ± 0.28) and 16 (3H/14C = 5.55 ± 0.3), respectively. These results show that during the C-24 methylation, H-24 is not lost; the hydrogen which is lost is located neither at C-24 nor at C-23 and must therefore be at C-25. This excludes routes a and b for sterol 12.
After incorporation of a mixture of [26,27-14C2]lanosterol and [23-3H]lanosterol (3H/14C = 4.36 ± 0.1) the isolated sterols 11a and 12a were converted into 11b (3H/14C = 4.12 ± 0.2) and 14b (3H/14C = 3.32 ± 0.14); a fraction of 12 was degraded into 15 (3H/14C = 2.28 ± 0.31) and 16 (3H/14C = 3.44 ± 0.15).
These results show that during the conversion of 13 into 12a, 50% of the H-23 atoms migrate from C-23 to C-24 and 25% remain on C-23; the other 25% are eliminated. During the conversion of 13 into 11a both H-23 atoms are retained. These results excluded route g for the two sterols. Since we have demonstrated that the conversion of 11c into 12a is possible in high yields (4.6%) with an efficiency eight times greater than the conversion of 12a into 11a, we propose that the sterol 11a is synthesized in vivoaccording to route e with migration of H-23 from C-23 to C-24. The sterol 12a is biosynthetized either by route d, f, the 22,23 double bond being introduced during the alkylation step, or by desaturation of the sterol 11a the C-22, C-23 double bond being introduced after the C-24 alkylation.
12 citations